In a medical context, the labelcolitis (without qualification) is used if:
The cause of the inflammation in the colon is undetermined; for example,colitis may be applied toCrohn's disease at a time when thediagnosis is unknown, or
The context is clear; for example, an individual withulcerative colitis is talking about their disease with a physician who knows thediagnosis.
Symptoms suggestive of colitis are worked up by obtaining themedical history, a physical examination, and laboratory tests (CBC,electrolytes, stool culture and sensitivity, stool ova and parasites, et cetera). Additional tests may include medical imaging (e.g. abdominalcomputed tomography,abdominal X-rays) and an examination with a camera inserted into the rectum (sigmoidoscopy,colonoscopy).[5]
An important investigation in the assessment of colitis is biopsy forhistopathology. A very small piece of tissue (usually about 2mm) is removed from the bowel mucosa during endoscopy and examined under the microscope by a histopathologist. A biopsy report generally does not state the diagnosis, but should state any presence of chronic colitis, give an indication of disease activity, as well as state the presence of any epithelial damage (erosions and ulcerations).[6]
Histopathology findings generally associated with chronic colitis include:[6]
Crypt degeneration
Crypt branching and other architectural distortions
Paneth cell (pictured) or gastric metaplasia (only applies in the left colon and rectum)
Other findings include basal plasmacytosis and mucin depletion.[6]Histopathology findings generally associated with active colitis include:[6]
Neutrophilic cryptitis (neutrophils within crypt epithelium)
Crypt abscesses (luminal neutrophilic aggregates)
Gland destruction
Ulceration (seen here as absence of epithelium, and granulation tissue with many fibroblasts)
A subtype of infectious colitis isClostridioides difficile colitis,[8] which is informally abbreviated as "C-diff colitis". It classically formspseudomembranes and is often referred to as pseudomembranous colitis, which is its (nonspecific)histomorphologic description.
Indeterminate colitis is the classification for colitis that has features of bothCrohn's disease andulcerative colitis.[10] Indeterminate colitis' behaviour is usually closer to ulcerative colitis than Crohn's disease.[11]
Treatment for this condition can include medications such assteroids and dietary changes. In some instances, hospitalization and surgery may be required.[12]
The use of oralprobiotic supplements to modify the composition and behavior of the microbiome has been considered as a possible therapy for both induction and maintenance of remission in people with Crohn's disease and ulcerative colitis. A Cochrane review in 2020 did not find clear evidence of improved remission likelihood, nor lower adverse events, in people with Crohn's disease, following probiotic treatment.[16]
For ulcerative colitis, there is low-certainty evidence that probiotic supplements may increase the probability of clinical remission.[17] People receiving probiotics were 73% more likely to experience disease remission and over 2x as likely to report improvement in symptoms compared to those receiving a placebo, with no clear difference in minor or serious adverse effects.[17] Although there was no clear evidence of greater remission when probiotic supplements were compared with5‐aminosalicylic acid treatment as amonotherapy, the likelihood of remission was 22% higher if probiotics were used in combination with 5-aminosalicylic acid therapy.[17] Whereas in people who are already in remission, it is unclear whether probiotics help to prevent future relapse, either as a monotherapy orcombination therapy.[18]
Additional research was conducted by Huanget al. that analyzed specific genes and biological markers that are associated with the risk of colon cancer development in patients with colitis. The results showed a correlation between certain biomarkers and the development of disease.[20]
Colitis is common in parts of the world wherehelminthic colonisation is rare, and uncommon in those areas where most people carry worms.Infections with helminths may alter the autoimmune response that causes the disease. Early trials ofTrichuris suis ova (TSO) showed promising results when used in people with IBD[21][22][23][24] but later trials failed at Phase 2, and most were eventually discontinued.[25] However, the phase 2 trials had used a different formulation of TSO from the one that had been used in the earlier studies that had shown positive outcomes.[26]
^Beutin L (September 2006). "Emerging enterohaemorrhagic Escherichia coli, causes and effects of the rise of a human pathogen".Journal of Veterinary Medicine. B, Infectious Diseases and Veterinary Public Health.53 (7):299–305.doi:10.1111/j.1439-0450.2006.00968.x.PMID16930272.
^Romano C, Famiani A, Gallizzi R, Comito D, Ferrau' V, Rossi P (December 2008). "Indeterminate colitis: a distinctive clinical pattern of inflammatory bowel disease in children".Pediatrics.122 (6):e1278 –e1281.doi:10.1542/peds.2008-2306.PMID19047226.S2CID1409823.
^Melton GB, Kiran RP, Fazio VW, He J, Shen B, Goldblum JR, et al. (October 2010). "Do preoperative factors predict subsequent diagnosis of Crohn's disease after ileal pouch-anal anastomosis for ulcerative or indeterminate colitis?".Colorectal Disease.12 (10):1026–1032.doi:10.1111/j.1463-1318.2009.02014.x.PMID19624520.S2CID44406331.
^Sun J, Lin J, Parashette K, Zhang J, Fan R (February 2015). "Association of lymphocytic colitis and lactase deficiency in pediatric population".Pathology, Research and Practice.211 (2):138–144.doi:10.1016/j.prp.2014.11.009.PMID25523228.
^Parker W (December 2017). "Not infection with parasitic worms, but rather colonization with therapeutic helminths".Immunology Letters.196:104–105.doi:10.1016/j.imlet.2017.07.008.PMID28720335.
